The invention relates to a heart valve prosthesis, used to replace diseased natural heart valves, and more particularly to a mechanical heart valve prosthesis that uses one or more naturally-operating pivoting members.
Various types of heart valve prostheses have been developed which operate hemodynamically as a result of the pumping action of the heart in which they generally function as check valves. These prosthetic valves fall generally into two categories: xe2x80x9cmechanicalxe2x80x9d valves, comprising relatively rigid leaflets formed of a stiff, biocompatible substance such as pyrolitic carbon; and xe2x80x9cbioprostheticxe2x80x9d valves, comprising flexible leaflets often formed of a biological material such as bovine pericardial tissue. One popular design for a mechanical heart valve prosthesis includes an annular valve body in which a pair of opposed leaflet occluders are pivotally mounted. The occluders move between a closed, mated position, blocking blood flow in an upstream direction, thereby minimizing regurgitation, and an open position, allowing blood flow in a downstream direction.
Typically, after receiving a mechanical heart valve prosthesis, the recipient must take chronic anticoagulation treatment for the rest of their life to prevent blood clots. These blood clots are referred to as thrombosis if they adhere to the heart valve. If the clots float away from the valve where they can occlude blood flow to another part of the body, the clots are referred to as thromboembolism. Thrombosis, thromboembolism, and bleeding that results from the drugs that are used to reduce cases of thrombosis and thromboembolism are the most serious problems faced by heart valve recipients. In contrast, after receiving a biological heart valve, the recipient typically only needs the chronic anticoagulation therapy for about ninety days while the sewing ring heals over.
To explain why blood clots occur more frequently in mechanical valve prostheses, scientists often look to the teachings of Verchow, an important nineteenth century scientist, who believed that clotting of the blood, or thrombosis, was the result of three interacting variables. These variables, often referred to as Verchow""s triad, include: (1) the susceptibility of a patient""s blood to clot formation; (2) foreign material response; and (3) flow conditions.
The susceptibility of a patient""s blood to clot formation can be diagnosed to a limited extent. Patients with particular susceptibility to clot formation may require anticoagulation even without the added risk of a prosthetic heart valve to avoid atrial and peripheral thrombosis. However, in the absence of anticoagulation treatment, mechanical valves generally give rise to greater clotting problems than bioprosthetic valves.
According to Verchow, areas of stasis, or low flow, are the most likely accumulation points for clots. For this reason, clots in prosthetic valves usually occur at the point where the sewing ring joins other valve members, or in low flow regions near struts and pivot points. Considerable effort has been directed at eliminating these low flow regions as discussed in U.S. Pat. Nos. 5,147,390 and 5,192,313. Although such attention to flow is likely to reduce the chance of valvular thrombosis, it does not explain the cause for heightened sensitivity to clot formation. Most tissue valves have many areas of blood stasis that are much worse than the pivots and struts in mechanical heart valves yet thrombosis is much less likely to occur in tissue valves than in mechanical valves, in the absence of anticoagulation therapy.
Since low flow does not explain the clotting risk difference between tissue and mechanical valves, a great deal of work has gone into investigating high flow rate effects on blood. High flow rates have been shown to cause damage to blood and to activate clotting mechanisms. In particular, high wall shear stress occurs where a rapidly moving flow meets an immobile boundary, like the walls of a heart valve or blood vessel. This high wall shear stress can cause blood damage. Michael T. H. Brodeur, M. D., et al., Red Blood Cell Survival In Patients With Aortic Valvular Disease and Ball-Valve Prostheses, XXXII Circulation 570 (1995); Richard M. Rubinson, M. D., et al., Mechanical Destruction of Erythrocytes By Incompetent Aortic Valvular Prostheses-Clinical, Hemodynamic, And Hematologic Findings, Am. Heart J. 179 (February 1966); Charles G. Nevaril, et al., Erythrocyte Damage And Destruction Induced By Shearing Stress, J. Lab and Clin. Med. 784 (May 1968).
Damage to the blood can also be caused by a rapid change in blood velocity, even in the absence of an impinging wall, particularly if the flow is turbulent. A. R. Williams, Viscoelasticity Of The Human Erythrocyte Membrane, 10 Biorheology 313-19 (1973); Paul D. Stein and Hani N. Sabbah, Measured Turbulence And Its Effects On Thrombus Formation, 35 Circulation Research 608-14 (1974); R. S. Figliola and T. J. Mueller, On The Hemolytic And Thrombogenic Potential Of Occluder Prosthetic Heart Valves From In-Vitro Measurements, 103 Journal of Biomechanical Eng""g. 83-89 (1981); Ahmed M. Salam and Ned Hwang, Human Red Blood Cell Hemolysis In A Turbulent Shear Flow: Contribution Of Reynolds Shear Stresses, 21 Biorheology 783-797 (1984); L. J. Worzinger, et al., Platelet And Coagulation Parameters Flowing Millisecond Exposure To Laminar Shear Stress, 381-386.
Laser doppler anemometry has been used to measure the forward flow dynamics in various mechanical and tissue valves. D. D. Hanle, et al., Invitro Flow Dynamics Of Four Prosthetic Aortic Valves: A Comparative Analysis, 22 J. Biomechanics 597-607 (1989). The data from these studies has been used to estimate the shear stress related blood damage that occurs during forward flow. M. Giersiepen, et al., Estimation Of Shear Stress-Related Blood Damage In Heart Valve Prostheses-Invitro Comparison Of 25 Aortic Valves, 13 Int""l. J. of Artificial Organs 306-330 (1990). In these reports, the shear stress and estimated damage to blood components with tissue valves is greater than the damage estimated from modern bileaflet mechanical valves during forward flow. The most recent reference even provides clinical comparative data supporting the fact that more hemolysis (risk of thrombosis) is indicated with tissue valves than with mechanical valves. There is also no evidence to suggest small valves are more prone to clotting than large valves, but both wall shear stresses and Reynolds normal stress are much higher in small valves than in large valves. These facts taken together indicate hemolysis is not a good indicator of the increased risk of clot formation with clinical valves, and the differences between the thromboembolic potential of tissue and mechanical valves is not related to forward flow dynamics.
Another possible link between clotting and flow conditions is the existence of high wall stresses or Reynolds normal stress associated with reverse flow leakage after the valve closes. Reynolds stresses on the order of 20,000 to 60,000 dynes/cm2 have been observed within the regurgitate jets occurring through a Bjork-Shiley valve mounted in a Penn-State heart. Baldwin, J. T., et al., Estimation Of Reynolds Stresses Within The Penn State Left Ventricular Assist Device, 36 ASAIO Trans. M274-M278 (1990); Baldwin, J. T., et al., Mean Velocities And Reynolds Stresses Within Regurgitant Jets Produced By Tilting Disk Valves, 37 ASAIO Trans. M351-M353 (1991). The peak Reynolds normal stresses during forward flow are on the order of 1,000 to 4,500 dynes/cm2, much lower than the Reynolds stresses during flow leakage. These higher stresses during leakage flow could be causing activation of the clotting system but high velocity jets are not unique to mechanical heart valves. Biological heart valves are often designed with a small leak in the center of the valve that results in a high velocity jet. Further, as biological valves degrade jets are created at tears and small holes that progress to complete valvular incompetence. If the high velocity leakage jets were a significant cause of activation then biological valves with central leakage would have a higher risk of clotting then biological valves without these jets but no such correlation exists. Also, if such jets were a primary cause of activation there would be an increased risk of clot formation as biological valves failed but this has not been reported.
Wall shear stress inside the pivots is another possible cause of blood damage. Empirical testing methods to determine the wall shear stress inside a heart valve pivot have not been developed but computational methods allow us to estimate these forces. In computational fluid dynamic (CFD) analysis of pivots exposed to pressure gradients of 120 mm of mercury, the flow inside the pivot has been characterized. This flow is laminar rather than turbulent and the wall shear stresses are below 300 dynes/cm2.
The extent of damage to the blood is also dependent on the surface roughness of the immobile surface and perhaps the surface chemistry of the impinging surface. Rougher surfaces are generally associated with increase thrombosis risk but polished pyrolitic carbon, titanium and cobalt chromium alloys used to fabricate mechanical heart valves are much smoother than the biological tissue used to fabricate tissue heart valves. In terms of surface chemistry, the glutaraidehyde treated tissue used to construct most tissue heart valves is toxic to some cells in the blood. Pyrolitic carbon, used for most mechanical heart valves has in contrast been shown to elicit a benign response allowing a confluent layer of protein absorption that is thought to be very non-thrombogenic.
Despite the foregoing evidence, which suggests that, according to Virchow""s theory, mechanical valves should be less thrombogenic than tissue valves, the clinical advantage of tissue valves compared to mechanical valves in terms of thrombogenicity is undisputed. Most recently, a study conducted by a group of surgeons and cardiologists in Aahurs, Denmark showed thirty-eight out of forty patients receiving the mostly widely used mechanical valve (St. Jude) had a measurable increased risk of thrombosis as compared to patients receiving tissue valves.
Recently experiments have been conducted which indicate that during the pumping cycle of the heart, mechanical valves experience rapid, relatively high magnitude pressure changes on the upstream or inlet side of the valve. In particular, immediately following the closure of the valve leaflets, rapid, short duration decreases in local pressure on the order of 750 mmHg have been measured. Accordingly, as used herein, the term xe2x80x9cpressure transientxe2x80x9d refers to a rapid, relatively large ( greater than 50 mmHg) pressure change of short duration ( less than 0.1 sec) at a point immediately upstream of the valve inlet at the moment of valve closure. Because the pressure is falling during these pressure changes, they are also referred to as xe2x80x9cnegative pressure transients.xe2x80x9d Significantly, tissue valves have not been show to experience negative pressure transients.
In one series of experiments involving negative pressure transients, tissue valves and mechanical valves with pressure transducers adjacent to the valves were implanted into sheep. Negative pressure transients on the order of 750 mmHg were measured upon valve closure with mechanical valves having pyrolytic carbon leaflets. In contrast, the magnitude of the negative pressure change with biological valves was less than 50 mmHg. Although outside the scope of Verchow""s theory, there has been work that indicates exposure of blood to rapid pressure transients can cause activation of blood leading to thrombosis. I believe the principle cause of thrombosis in mechanical heart valves is the result of the pressure transient that exists with mechanical valves but is absent with tissue valves. This invention is directed at elimination or at least reduction of this pressure transient by moving the valve to a closed position before the blood is exposed to substantial pressure gradients.
Without being bound by any particular theory, it is believed that the negative pressure transients experienced by most mechanical heart valves occurs as follows. During the closing cycle of a typical mechanical heart valve having pyrolytic carbon leaflets, the volume of blood backflowing through the valve decreases as more of the fluid passageway is occluded by the closing leaflets. However, the velocity (and thus kinetic energy) of the remaining blood backflowing through the valve actually increases as the passageway area decreases. Thus, for a typical bileaflet valve, immediately prior to complete valve closure an extremely high-velocity backflow jet exists at the periphery of the valve leaflets. When the leaflets close fully, the kinetic energy (inertia) of this jet cause it to continue to backflow for a small time interval, resulting in a highly localized negative pressure transient as the small volume of blood is decelerated and stopped. This negative pressure transient can cause a viscoelastic expansion of blood cells, releasing granular material through the cell walls and resulting in an increase in the risk of thrombosis. In extreme cases the cells can be torn, releasing substantial quantities of thrombogenic granular material.
It has previously been suggested in published PCT application number WO/30658 to use magnetic forces in a heart valve assembly to move the leaflets to an equilibrium position that is between the open and closed positions when a zero pressure gradient exists across the valve. As taught by this reference, the purpose in doing this is to minimize the distance the leaflet must travel from this equilibrium position to both the open and closed position, and also to reduce reflux. WO/30658, however, does not recognize or discuss the importance of the exposure of blood to pressure transients, and the device described therein does not achieve the objective of reducing or eliminating the exposure of blood to such closing pressure transients. In fact, an equilibrium position that is between the open and closed positions ensures that the blood will be exposed to global pressure transients of a magnitude sufficient to cause blood flow reversal. As indicated in the publication, both opening and closing of the valve will always take place in two steps, the first being under the influence of magnetic forces, and the second being under the influence of hydraulic forces that result from a global pressure transient.
To the contrary the valve of the present invention substantially eliminates the exposure of blood to closing pressure transients by using a biasing force, such as a mechanical or magnetic force, to move the valve to the closed position when a zero pressure gradient exists across the valve. Moving the valve to a closed position will substantially eliminate the exposure of blood to a closing pressure transient, and therefore, will reduce the risk of thrombosis. The present invention has the further advantage of substantially eliminating closing volume reflux, resulting in a more efficient valve that more closely mimics the performance of a natural heart valve.
In general, in one aspect, the invention features a heart valve prosthesis. The prosthesis includes an annular body that has a fluid passageway through it and at least one rigid leaflet that is pivotally mounted in the passageway of the body. The leaflet is movable between a closed position in which the fluid passageway is substantially closed and an open position in which the fluid passageway is not closed. A biasing mechanism that is connected to the body and the leaflet exerts a biasing force to bias the leaflet to the closed position. The leaflet is configured to move to the open position when a first fluid pressure exerted on an inflow surface of the leaflet exceeds the biasing force. It is also configured to return to the closed position sooner than prior art valves, preferably before a second fluid pressure exerted on an outflow surface of the leaflet exceeds the first fluid pressure, in contrast to existing art valves that close only after flow reverses and the pressure from a second fluid force on the outflow side of the valve exceeds the first pressure force.
An advantage of the present invention is that the prosthetic valve will fully close under a very low closing pressure transient, thereby reducing damage to blood. In preferred embodiments, the negative pressure transient is reduced to 700 mmHg or less, more preferably to 500 mmHg or less, even more preferably to 250 mmHg or less, and more preferably still to 100 mmHg or less. The valve closes slowly during deceleration of forward flow, thereby minimizing the noise made by the valve that frequently annoys valve recipients. Since the valve will close earlier in the cardiac cycle than prior art valves, the present invention will also substantially reduce or eliminate the closing volume or energy loss associated with retrograde blood flow that results with valves that depend on a flow reversal to close the valve.
As indicated, the mechanism of the invention may be configured to move the leaflet to the closed position when the first fluid pressure is insufficient to overcome the magnetic or mechanical biasing force that is holding the valve closed. The mechanism may include a first magnet that is mounted to the leaflet and a second magnet that is mounted to the orifice body or in the space between the orifice body and stiffening ring or sewing ring. The first and second magnets may be configured to attract each other when the leaflet is in the closed position. The first and second magnets may be configured to repel each other when the leaflet is in the open position. The open position may define a predetermined maximum angular position of the leaflet, and the first and second magnets may be configured to prevent the leaflet from traveling substantially beyond the open position. Alternatively, instead of magnets, the valve prostheses may include a spring. The heart valve prosthesis may be a mechanical bileaflet heart valve prosthesis.
In general, in another aspect, the invention features a heart valve prosthesis that includes an annular body that has a fluid passageway and at least one leaflet that is pivotally mounted in the passageway of the body and is movable between a closed position in which the fluid passageway is closed and an open position in which the fluid passageway is not closed. The heart valve prosthesis also includes a first biasing element mounted to the leaflet and a second biasing element mounted to the body. The second biasing element is configured to interact with the first biasing element to exert a force on the leaflet to move the leaflet to the closed position before the valve experiences a negative pressure transient of 700 mmHg. More preferably, the leaflet is moved to the closed position before the valve experiences a negative pressure transient of 500 mmHg. Even more preferably, the leaflet is closed before the valve experiences a negative pressure transient of 250 mmHg. More preferably still, the leaflet is closed before the valve experiences a negative pressure transient of 100 mmHg. It is also preferred that the leaflet be moved to the closed position before a second fluid pressure exerted on an outflow surface of the leaflet exceeds a first fluid pressure exerted on an inflow surface of the leaflet.
In general, in another aspect, the invention features a method for use with a heart valve prosthesis that has a fluid passageway and at least one leaflet that is located in the passageway and that is similarly movable between a closed position in which the fluid passageway is substantially closed and an open position in which the fluid passageway is not substantially closed. The method includes mounting a biasing element on the leaflet and applying magnetic force to the element to force the leaflet to the closed position before a second fluid pressure exerted on an outflow surface of the leaflet exceeds a first fluid pressure exerted on an inflow surface of the leaflet.
In general, in another aspect, the invention features a method for use with a heart valve prosthesis that has a fluid passageway and at least one leaflet that is located in the passageway and that is similarly movable between a closed position in which the fluid passageway is substantially closed and an open position in which the fluid passageway is not substantially closed. The method includes mounting a biasing element on the leaflet and applying magnetic force to the element to force the leaflet to the closed position before the valve experiences a negative pressure transient of 700 mmHg. More preferably, the leaflet is moved to the closed position before the valve experiences a negative pressure transient of 500 mmHg. Even more preferably, the leaflet is closed before the valve experiences a negative pressure transient of 250 mmHg. More preferably still, the leaflet is closed before the valve experiences a negative pressure transient of 100 mmHg.
In general, in another aspect, the invention features a replacement heart valve that includes a valve body and a leaflet mounted in the body for pivoted rotation about an axis between open and closed positions. The leaflet does not impact against a stop in the open position.
Other advantages and features will become apparent from the following description and from the claims.